Breastfeeding benefits heart health

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Hi All,

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This is another of the studies demonstrating the potential benefit of

breastfeeding. Breastfeeding is good for heart health in later life,

it

seems. That it is a prospective study of long duration may increase

the

significance.

The pdf is available.

Definitions are:

breast feeding: The ability of the breast to produce milk diminishes

soon

after childbirth without the stimulation of breastfeeding. Immunity

factors

in breast milk can help the baby to fight off infections. Breast milk

contains vitamins, minerals, and enzymes which aid the baby's

digestion.

Breast and formula feeding can be used together.

intima: Inner layer of blood vessel, comprising an endothelial

monolayer

on the luminal face with a subcellular elastic extracellular matrix

containing a few smooth muscle cells. Below the intima is the media,

then

the adventitia.

atherosclerosis: The progressive narrowing and hardening of the

arteries

over time. This is known to occur to some degree with aging, but

other risk

factors that accelerate this process have been identified. These

factors

include: high cholesterol, high blood pressure, smoking, diabetes and

family history for atherosclerotic disease.

Arterioscler Thromb Vasc Biol. 2005;25:1482-1488.

RM, Ebrahim S, M, Davey G, Nicolaides AN,

Georgiou N,

S, el S, Holly JM, Gunnell D.

Breastfeeding and atherosclerosis: intima-media thickness and plaques

at 65-

year follow-up of the Boyd Orr cohort.

Arterioscler Thromb Vasc Biol. 2005 Jul;25(7):1482-8. Epub 2005 May

12.

PMID: 15890972

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=15890972 & query_hl=43

Abstract

Objectives—: The impact of breastfeeding in infancy on cardiovascular

disease risk is uncertain. We related breastfeeding in infancy to

atherosclerosis in adulthood.

Methods and Results—: A historic cohort study based on a 65-year

follow-

up ... 1937 to 1939. A total of 732 eligible cohort members ... were

invited for follow-up examinations in 2002, and 405 (55%)

participated. In

models controlling for age and sex, breastfeeding was inversely

associated

with common carotid intima-media thickness (IMT; difference -0.03 mm;

95%

CI, -0.07 to 0.01), bifurcation IMT (difference -0.19 mm; 95% CI, -

0.37 to -

0.01), carotid plaque (odds ratio [OR], 0.52; 95% CI, 0.29 to 0.92),

and

femoral plaque (OR, 0.54; 95% CI, 0.26 to 1.12), compared with bottle-

feeding. Controlling for socioeconomic variables in childhood and

adulthood, smoking and alcohol made little difference to effect

estimates.

Controlling for factors potentially on the causal pathway (blood

pressure,

adiposity, cholesterol, insulin resistance, and C-reactive protein)

made

little difference to observed associations.

Conclusions—: Breastfeeding may be associated with a reduced risk of

atherosclerosis in later life. Measurement error and power

considerations

limit the extent to which conclusions about the mechanisms underlying

this

relationship can be made.

.... Results

Overall, 182 (45%) men and 223 (55%) women were followed up in

clinic, and

155 (46%) men and 184 (54%) women were scanned (Figure I). Their mean

age

was 71 years (range 63 to 82) with no sex difference (P=0.5). Method

of

infant feeding was available for 362 participants, of whom 272 (75%)

were

breastfed with no sex difference (P=0.7). The median duration of

breastfeeding was 9 months (interquartile range [iQR], 5 to 9) in

both

sexes (P=0.7). This is similar to the prevalence (70%) and median

duration

(9 months; IQR, 4 to 9) of breastfeeding in the full cohort.20

Breastfed

subjects were 284 g (95% CI, 65 to 503) heavier at birth, but there

was

little difference in infant feeding mode by age, year born, sex,

childhood

social class, food expenditure, nutrient intake, adult social class,

smoking, or alcohol use (Table I, available online at

http://atvb.ahajournals.org ).

Representativeness

Compared with the remaining surviving survey members (n=2563), clinic

participants were 10 months younger at baseline (95% CI, 4 to 14

months),

taller (difference in height z score, 0.19; 95% CI, 0.07 to 0.32),

more

likely to have been breastfed (75% versus 69%), and when they were

children, the family per-capita weekly food expenditure was >5

shillings

(ie, 25 pence, equivalent to £12.16 at current prices) among 55% of

participants versus 41% of nonparticipants. Birth year, sex, birth

weight,

father's social class, and childhood body mass index (BMI) were

similar

whether subjects were followed up or not.

Cardiovascular Disease Risk Factors

In general, there was little evidence of differences in risk factors

(adiposity, blood pressure, lipids, or insulin resistance) between

breastfed and bottle-fed participants (Table 1). There was some

evidence

that breastfeeding was associated with lower average glycemia

measured by

hemoglobin A1c (HbA1c) in those without diabetes (difference -0.07%;

95%

CI, -0.17 to 0.02). In models controlling for age, sex,

socioeconomic, and

behavioral factors and BMI, the difference in HbA1c between breastfed

and

bottle-fed subjects was -0.12% (95% CI, -0.26 to 0.02; P=0.1) in all

subjects and -0.10% (95% CI, -0.19 to 0.00; P=0.05) in subjects

without

diabetes. There was no evidence of an association of breastfeeding

with

type 2 diabetes (odds ratio [OR], 0.97; 95% CI, 0.41 to 2.30; P=0.9).

There

was some evidence of a reduction in odds of being on an

antihypertensive

drug associated with breastfeeding (OR, 0.67; 0.40 to 1.12; P=0.1).

TABLE 1. Distribution of Cardiovascular Disease Risk Factors by

Infant

Feeding Mode

.........................................

CHD Risk Factor n (clusters*)----Mean (SD)----

------------Breastfed Bottle-Fed----Mean Difference † (95% CI;

(breastfed –

bottle-fed)

........................................

Adiposity

BMI (kg/m 2 ) 362 (277) 27.45 (4.34) 27.47 (4.69) 0.01 (–1.07 to

1.08);

P=0.9

Fat mass index (kg/m 2 ) 362 (277) 9.37 (3.40) 9.42 (3.16) 0.06 (–

0.66 to

0.78); P=0.9

Lean mass index (kg/m 2 ) 362 (277) 18.09 (2.13) 18.05 (2.58) –0.02

(–0.48

to 0.43); P=0.9

Fat mass percent 362 (277) 33.27 (7.93) 33.67 (7.18) –0.04 (–1.44 to

1.36); P=0.9

Waist/hip ratio 361 (276) 0.907 (0.092) 0.912 (0.097) –0.008 (–0.027

to

0.010); P=0.4

Waist/thigh ratio 361 (277) 1.815 (0.218) 1.842 (0.214) –0.031 (–

0.076 to

0.015); P=0.2

Blood pressure

Systolic (mm Hg) 362 (277) 147.78 (21.79) 149.02 (23.60) –1.62 (–

6.66 to

3.41); P=0.5

Diastolic (mm Hg) 362 (277) 82.78 (10.29) 83.24 (9.60) –0.74 (–3.06

to

1.57); P=0.5

Lipid profile

Total cholesterol (mmol/L) 362 (277) 5.75 (1.21) 5.68 (1.16) 0.12 (–

0.15 to

0.40); P=0.4

HDL cholesterol (mmol/L) 362 (277) 1.57 (0.42) 1.60 (0.45) –0.01 (–

0.11 to

0.09); P=0.8

LDL cholesterol (mmol/L) 362 (277) 3.52 (1.08) 3.40 (0.94) 0.16 (–

0.09 to

0.41); P=0.2

Triglyceride (mmol/L) ‡ 362 (277) 1.32 (0.42) 1.36 (0.45) –0.02 (–

0.13 to

0.08); P=0.7

hs-CRP (mg/L) ‡ 362 (277) 2.04 (1.01) 2.17 (1.14) –0.06 (–0.31 to

0.19);

P=0.7

Glycemia/insulin resistance

Insulin (mU/L) ‡ 314 (240) 8.00 (0.59) 8.08 (0.60) –0.02 (–0.17 to

0.13);

P=0.8

Insulin resistance (HOMA) ‡ 313 (239) 1.90 (0.62) 1.94 (0.63) –0.03

(–0.19

to 0.13); P=0.7

HbA1c (%), all participants # 360 (275) 5.74 (0.58) 5.82 (0.67) –

0.08 (–

0.23 to 0.06); P=0.3

HbA1c (%), participants not receiving antidiabetic treatment 334

(255) 5.63

(0.38) 5.70 (0.45) –0.07 (–0.17 to 0.02); P=0.1

.............................................

hs-CRP indicates high-sensitivity C-reactive protein; HOMA,

homeostasis

model assessment.

*The cluster unit was the family.

†All models for mean differences based on random-effects linear

regression

and control for sex and age; all models except

biochemistry also control for the hour of the examination and field

observer; all models with blood pressures as outcomes control,

in addition, for arm circumference, room temperature, and the Omron

machine

used.

‡Values were log transformed; geometric means and logged regression

coefficients are presented.

#Two subjects with outlying HbA1c values were omitted.

Atherosclerosis

In line with other population-based studies,14 the common carotid IMT

was

normally distributed with means (SD) of 0.79 (0.18) and 0.72 (0.13)

mm for

men and women, respectively; the mean (SD) bifurcation IMT was 1.82

(0.78)

and 1.63 (0.69) mm for men and women, respectively. In age- and sex-

adjusted models, breastfeeding was associated with reductions in

bifurcation IMT (difference, -0.19; 95% CI, -0.37 to -0.01) and odds

of

carotid plaque (OR, 0.52; 95% CI, 0.29 to 0.92; Table II, available

online

at http://atvb.ahajournals.org ).

In models controlling for age, sex, and socioeconomic and behavioral

factors, breastfeeding was associated with reductions in common

carotid

(difference -0.03 mm; 95% CI, -0.07 to 0.01) and bifurcation (-0.23

mm; 95%

CI, -0.40 to -0.06) IMT compared with bottle-feeding (Table 2).

Breastfeeding was also associated with reductions in odds of carotid

(OR,

0.45; 0.24 to 0.86) and femoral (0.46; 95% CI, 0.21 to 1.01) plaques

(Table

3). Further adjustment for cardiovascular disease risk factors hardly

altered the effect estimates, except HbA1c, which attenuated the

association between breastfeeding and bifurcation IMT by 13%.

TABLE 2. Association of Breastfeeding With Carotid and Bifurcation

IMT

Controlling for Potential Confounding Variables and Risk Factors for

Coronary Heart Disease

.....................................

Cumulative Adjustment-------Mean Difference, mm † (95% CI; breastfed –

bottle-fed)

------------------------Common Carotid IMT (n=306) Bifurcation IMT

(n=306)

.....................................

Age and sex –0.03 (–0.07 to 0.01); P=0.1 –0.19 (–0.37 to –0.01);

P=0.04

Age, sex, and socioeconomic ‡ factors –0.03 (–0.07 to 0.01); P=0.1 –

0.24

(–0.41 to –0.06); P=0.009

Age, sex, socioeconomic ‡ and behavioral # factors –0.03 (–0.07 to

0.01);

P=0.1 –0.23 (–0.40 to –0.06); P=0.009

Age, sex, and socioeconomic ‡ and behavioral # factors

+Systolic blood pressure –0.03 (–0.06 to 0.01); P=0.2 –0.23 (–0.40

to –

0.06); P=0.009

BMI –0.03 (–0.07 to 0.01); P=0.1 –0.23 (–0.40 to –0.06); P=0.008

+Waist/hip ratio –0.03 (–0.07 to 0.01); P=0.1 –0.22 (–0.39 to –

0.05);

P=0.01

+Total cholesterol –0.03 (–0.07 to 0.01); P=0.1 –0.22 (–0.39 to –

0.05);

P=0.01

+High-sensitivity C-reactive protein ** –0.03 (–0.07 to 0.01);

P=0.1 –

0.23 (–0.40 to –0.06); P=0.009

+HOMA insulin resistance ** –0.03 (–0.07 to 0.01); P=0.1 –0.22 (–

0.39

to –0.05); P=0.01

+HbA1c –0.02 (–0.06 to 0.01); P=0.2 –0.20 (–0.37 to –0.03); P=0.02

...................................................

---------Regression Coefficients From the Above Models (95% CI)

Relating

Risk Factors With IMT*

................Common Carotid IMT Bifurcation IMT----

.................................................

Smoking (current or past vs never) 0.02 (–0.02 to 0.05); P=0.4 0.27

(0.11

to 0.43); P=0.001

Systolic blood pressure (per 10 mm Hg) 0.02 (0.01 to 0.03); P0.001

0.03 (–

0.01 to 0.07); P=0.1

BMI (per quintile) 0.01 (0.00 to 0.02); P=0.05 0.04 (–0.02 to 0.09);

P=0.2

Waist/hip ratio (per quintile) 0.00 (–0.01 to 0.01); P=0.9 0.06 (0.00

to

0.13); P=0.07

Total cholesterol (per mmol/L) 0.01 (–0.01 to 0.02); P=0.3 –0.05 (–

0.12 to

0.02); P=0.2

High-sensitivity C-reactive protein (per quintile) 0.01 (0.00 to

0.02);

P=0.2 0.06 (0.01 to 0.11); P=0.03

HOMA (per quintile) 0.00 (–0.01 to 0.02); P=0.6 0.03 (–0.02 to 0.09);

P=0.3

HbA1c (per %) 0.03 (0.01 to 0.05); P=0.008 0.14 (0.04 to 0.24);

P=0.004

................................................

†Based on random-effects linear regression models.

‡Father's social class, birth order, household food expenditure in

childhood, social class in adulthood, and area where the clinic

survey was undertaken.

#Smoking and alcohol consumption in adulthood (models with alcohol

and

smoking were based on 304 subjects because of

missing data).

+Extra variable in model in addition to age, sex, and socioeconomic

and

behavioral factors.

**Entered as logged variables.

*Regression coefficients are change in IMT (mm) per unit increase in

risk

factor.

HOMA indicates homeostasis model assessment.

TABLE 3. Association of Breastfeeding With Carotid and Femoral

Plaques

Controlling for Potential Confounding Variables and Risk Factors for

Coronary Heart Disease

.....................................................

Cumulative Adjustment---OR (95% CI †; breastfed vs bottle fed)---

--------------------------Carotid Plaques (n=306) Femoral Plaques

(n=306)

.....................................................

Age and sex 0.52 (0.29 to 0.92); P=0.03 0.54 (0.26 to 1.12); P=0.1

Age, sex, and socioeconomic ‡ factors 0.47 (0.25 to 0.88); P=0.02

0.47

(0.22 to 1.04); P=0.06

Age, sex, and socioeconomic ‡ and behavioral # factors 0.45 (0.24 to

0.86); P=0.02 0.46 (0.21 to 1.01); P=0.05

Age, sex, and socioeconomic ‡ and behavioral # factors

+Systolic blood pressure 0.44 (0.23 to 0.84); P=0.01 0.46 (0.21 to

1.00);

P=0.05

+BMI 0.44 (0.23 to 0.84); P=0.01 0.45 (0.20 to 0.99); P=0.05

+Waist/hip ratio 0.45 (0.24 to 0.86); P=0.02 0.45 (0.20 to 1.00);

P=0.05

+Total cholesterol 0.46 (0.24 to 0.87); P=0.02 0.46 (0.20 to 1.02);

P=0.06

+High-sensitivity C-reactive protein ** 0.45 (0.24 to 0.86); P=0.02

0.42

(0.18 to 0.99); P=0.05

+HOMA insulin resistance ** 0.45 (0.24 to 0.86); P=0.02 0.46 (0.21 to

1.01); P=0.05

+HbA1c 0.50 (0.26 to 0.96); P=0.04 0.45 (0.20 to 1.00); P=0.05

......................................................

--------------ORs (95% CI †) Relating CVD Risk Factors With Plaque

Prevalence From the Above Models*

---------------Carotid Plaques (n=306) Femoral Plaques (n=306)----

............................................................

Smoking (current or past vs never) 1.54 (0.87 to 2.73); P=0.1 1.67

(0.95 to

2.94); P=0.08

Systolic blood pressure (per 10 mm Hg) 1.24 (1.08 to 1.42); P=0.003

1.07

(0.92 to 1.24); P=0.4

BMI (per quintile) 1.13 (0.93 to 1.37); P=0.2 1.08 (0.86 to 1.36);

P=0.5

Waist/hip ratio (per quintile) 1.36 (1.08 to 1.69); P=0.008 1.03

(0.79 to

1.33); P=0.9

Total cholesterol (per mmol/L) 0.81 (0.63 to 1.05); P=0.1 0.99 (0.77

to

1.27); P=0.9

High-sensitivity C-reactive protein (per quintile) 1.33 (1.10 to

1.61);

P=0.003 1.30 (1.05 to 1.61); P=0.02

HOMA (per quintile) 1.31 (1.06 to 1.62); P=0.01 0.93 (0.73 to 1.18);

P=0.6

HbA1c (per %) 1.71 (1.18 to 2.48); P=0.005 0.93 (0.65 to 1.34); P=0.7

.........................................

†Based on robust standard errors.

‡Father's social class, birth order, household food expenditure in

childhood, social class in adulthood, and area where the clinic

survey was undertaken.

#Smoking and alcohol consumption in adulthood (models with alcohol

and

smoking were based on 304 subjects because of

missing data).

+Extra variable in model in addition to age, sex, and socioeconomic

and

behavioral factors.

**Entered as logged variables.

*ORs are change in odds of plaque per unit increase in risk factor.

HOMA indicates homeostasis model assessment.

Neither birth weight (a marker for fetal growth), childhood leg

length (a

marker for childhood growth and adverse exposures during growth),21

nor

specific nutrient intakes in childhood confounded the breastfeeding–

atherosclerosis associations. There was little evidence of

interaction by

sex, age at examination, year of birth category, childhood BMI,

energy,

fat, or saturated fat intake. There was little evidence of a duration-

response relationship between breastfeeding and atherosclerosis

(Table III,

available online at http://atvb.ahajournals.org ). The mean

difference in

bifurcation IMT was 0.12 mm (95% CI, -0.04 to 0.28; P=0.16) and the

OR for

carotid plaques was 2.05 (95% CI, 1.03 to 4.08; P=0.04) per category

of

increasing breastfeeding duration (reference < 6 months of

breastfeeding).

There was little evidence of an association of breastfeeding with

self-

reported ischemic heart disease (OR, 0.88; 95% CI, 0.49 to 1.56;

P=0.7).

Breastfeeding-IMT (P interaction >0.5) and -plaque (P interaction

>0.1)

associations did not differ among those with and without clinical

evidence

of ischemia.

Sensitivity Analyses

When analyses were reweighted to assess the impact of missing data,

effect

sizes were little altered. In weighted models based on all 2563

surviving

nonrespondents in England, Wales and Scotland, inverse associations

of

breastfeeding with common carotid (difference -0.03; 95% CI: -0.07 to

0.01)

and bifurcation (difference -0.17; 95% CI, -0.4 to 0.03) IMT, carotid

(OR,

0.49; 95% CI, 0.25 to 0.99) and femoral plaques (OR, 0.62; 95% CI,

0.31 to

1.24) remained. Results were similar when analyses were repeated

using

study area nonrespondents.

Discussion

Breastfeeding was inversely associated with atherosclerosis, measured

by

IMT and plaque prevalence. We also observed a 0.12% reduction in

HbA1c in

breastfed versus bottle-fed subjects. Although of borderline

statistical

significance, the findings are of interest for at least 2 reasons.

First,

the differences in IMT and plaque prevalence associated with

breastfeeding

were of a similar magnitude to differences seen in smokers versus

never-

smokers and those with and without evidence of coronary heart

disease.14

The potential public health importance of the reduction in HbA1c

associated

with breastfeeding is suggested by the observation that lowering the

nondiabetic population mean HbA1c by just 0.1% has been predicted to

reduce

total mortality by 5%.22 Second, the decision to breastfeed in the

pre–

World War II era was less socially patterned than it is now,23

providing

some control for socioeconomic confounding at the design stage of

this

study. In contrast, breastfeeding mothers of children born during the

last

30 to 40 years are more educated and more health-conscious than

mothers who

bottle-feed,24 and the influence of possible confounding factors in

recent

studies of the long-term effects of breastfeeding is probably

impossible to

completely control for.25 The breastfeeding–atherosclerosis

associations

were independent of other early life factors, such as birth weight,

nutrition, and socioeconomic conditions in childhood, of

socioeconomic

environment in adulthood, and of factors (smoking and alcohol)

operating in

later life that may be related to healthy upbringing among children

of

mothers who breastfed.

We were unable to establish a mechanism by which breastfeeding may

influence atherosclerosis. We had hypothesized that any association

may

operate via blood pressure,2,9 cholesterol levels,1 glycemia, or

insulin

resistance,3,4 but effect estimates were only altered a little after

controlling for glycosylated hemoglobin. However, measurement error

may

account for this apparent lack of any substantial effect of

controlling for

these factors. Furthermore, we cannot exclude the possibility that

lifelong

exposure (as opposed to concurrent risk factor levels) to increased

blood

pressure, cholesterol levels, or insulin resistance may be underlying

mechanisms. Breastfeeding has been associated with a reduced

prevalence of

arterial plaques in children,8 and cardiovascular disease risk

factors

measured in childhood are prospectively associated with IMT in

adulthood,

independently of contemporaneous risk factors.26 Breastfeeding may be

more

strongly associated with blood pressure, cholesterol levels,

glycemia, or

insulin resistance much earlier in life, perhaps during the infant

feeding

period,1,27,28 protecting against early arterial damage.

Acute and chronic viral/bacterial infections have been associated

with

atherosclerosis, although the evidence is inconclusive.29 We could

not

investigate whether breastfeeding protects against atherosclerosis by

reducing exposure to persistent infections in infancy.23,30

.... Generalizability

Baboon studies suggest that infant feeding method may interact with a

diet

high in saturated fat in childhood to influence the development of

atherosclerosis.13 Given subspecies differences in the apolipoprotein

A

genetic variants and levels of lipoprotein A, and a lack of data from

other

primates, it is possible that these findings are specific for this

particular subspecies of baboon and thus have little relevance to

humans.36

However, an influence of breastfeeding in humans may depend on later

dietary patterns, which are now very different from those in the

early 20th

century.37 We found no interactions by childhood BMI, energy, fat, or

saturated fat intake on breastfeeding–atherosclerosis associations,

although power to detect these was limited.

Artificial feeds in the 1920s to 1930s were largely based on

unmodified

cow's milk.23 Unlike formula milks of today (low in cholesterol,

saturated

fatty acid, and sodium), unmodified cow's milk (unless it was

diluted) had

a high sodium concentration (low in breastmilk) but more closely

resembled

the cholesterol and saturated fatty acid content of mature

breastmilk.38

Distinct associations with particular components of artificial feeds

(such

as differences in salt content) may produce different results in

contemporary versus historic cohorts. Other differences between the

composition of breast milk and cow's milk and modern formula feeds in

hormones (eg, leptin and thyroxine), immunoglobulins, and nucleotides

might

be important.1 Altered hormonal responses to breast and formula

feeds, for

example, different insulin 27 and growth factor,39 effects may

explain

variations in outcomes in later life. We had no information on

breastfeeding exclusivity and do not know whether results differ

among

infants who were exclusively or partially breastfed.

Comparison With Other Studies

In line with our findings, a postmortem study in young adults found

lower

rates of coronary atheroma among those breastfed (25%) compared with

those

artificially fed (60%).8 In Hertfordshire, men who had been partially

or

exclusively breastfed <1 year had lower standardized mortality ratios

(SMRs; 73 and 79, respectively) compared with those who had been

exclusively breastfed for >1 year (SMR, 97) or exclusively bottle-fed

(SMR,

95).6 The results are in line with data from a recently published

study on

87 252 participants in the Nurses Health Study, born between 1921 and

1946.

Ever having been breastfed was associated with an 8% to 10% reduction

in

risk of coronary heart disease and stroke; the reduction in risk of

coronary heart disease was 16% for women breastfed >9 months.40

However,

other studies have found no association between breastfeeding and

coronary

artery plaques among young accident victims at postmortem,11 nonfatal

myocardial infarction,12 and cardiovascular or coronary heart disease

mortality.10 Small sample size 11,12 and selection bias 10 are a

concern

with these studies. We have shown recently no association of

breastfeeding

with ischemic heart disease mortality (hazard ratio, 1.02) in the

Boyd Orr

cohort.20 Although breastfeeding may influence subclinical

atherosclerosis,

other factors may be important for survival among those with disease.

The inverse relationship between breastfeeding and HbA1c, a measure

of

average glycemia, concurs with 2 studies showing lower levels of

impaired

glucose tolerance 3 and type 2 diabetes 4 in adult life among

breastfed

subjects. We observed differences in systolic and diastolic blood

pressure

of -1.62 mm Hg and -0.74 mm Hg, respectively, between breastfed and

bottle-

fed subjects, in line with a recent meta-analysis.2 However, the

current

study was only powered to detect differences of 6.5 mm Hg systolic

and 3.2

mm Hg diastolic blood pressure. Despite recent interest in the

relationship

between breastfeeding and obesity, our findings indicate no evidence

of any

such association.

Breastfeeding is associated with a reduction in atherosclerosis, but

the

mechanism is unclear. Prospective investigations of the association

between

breastfeeding and ischemic heart disease are lacking. Furthermore,

such

studies would have to be prohibitively large and long term to detect

small

but (on a population level) important reductions in ischemic heart

disease.

Approximately 40% of infants are never breastfed in the United

Kingdom.24

In the absence of prospective evidence, this study suggests the

possibility

that the promotion of breastfeeding could be a potential component of

the

public health strategy to reduce future levels of ischemic

cardiovascular

disease. However, further studies in large adult populations are

needed to

confirm these findings. In particular, the hypothesis that

breastfeeding

influences later cardiovascular disease risk factors could ethically

and

feasibly be tested on an intention-to-treat basis in large controlled

trials of successful breastfeeding promotion interventions with long-

term

follow-up.41